Pancreas Pathology Flashcards
1
Q
Agenesis
A
total absence; usually w/ widespread anomalies incompatible w/ life
2
Q
Ectopic/ Heterotopic Pancreas
A
(most common but usually benign)
- Normal pancreatic tissue in stomach, duodenum, jejunem, Meckel diverticulum, ileum
- Usually found incidentally but may cause pain from local inflammation; rarely causes mucosal bleeding;
- May see as sessile mass
3
Q
Annular Pancreas
A
- Ring of pancreas parenchyma around 2nd portion of duodenum
- Can cause duodenal obstruction –> gastric distension, vomiting, dbl bubble on imaging
4
Q
Pancreas Divisum
A
(most common clinically sig)
- Failure of dorsal and ventral ducts to merge properly –> majority of pancreas drained by duct of Santorini into minor papilla instead of using ampulla of Vater
- May predispose to chronic pancreatitis
5
Q
Pancreatic Cysts
A
- From anomalous development of pancreatic ducts
- Can be part of polycystic disease (also in kidney, liver)
- von Hippel Lindau Disease (also in kidney, liver + vascular neoplasms in retina and brainstem)
6
Q
What is acute pancreatitis? (+ common causes)
A
- REVERSIBLE
- Inflammation from digestive enzymes themselves
- Ranges from edema and fat necrosis –> parenchymal necrosis w/ severe hemorrhage
- Common etiologies: alcoholism, obstruction of bile ducts
7
Q
3 Possible Mechanisms of Acute Pancreatitis
A
- 1- pancreatic duct obstruction - leads to build up of pressure in intrapancreatic ducts; block ductal flow –> enzyme rich interstitial fluid (includes lipase in active form so damages local parenchyma) + cytokines released –> inc edema from leaky vasculature which now blocks local blood flow –> ischemic injury to acinar cells
- 2- Primary injury of acinar cells (by virus. drugs, direct trauma)
- 3- Defective intracellular transport - abberent packaging of digestive enzymes by acinar cells; alcohol or trauma –> intracellular activation of digestive enzymes –> released and cause acinar damage
8
Q
Pathology of Acute Pancreatitis
A
- Edema (vessel micro-leakage)
- Fat necrosis (by lipolytic enzymes like lipase)
- Saponification (alkaline hydrolysis of TGs –> FAs)
- Once more severe … necrosis of parenchyma and hemorrhage around areas of necrosis due to damage to vessels
9
Q
Chronic Pancreatitis Pathology
A
- Loss of lobular architecture
- Parenchymal fibrosis (reduced # and size of acini but Islets spared)
- Acinar loss
- Dilated ducts w/ chronic inflammatory infiltrate around ducts and lobules (plasma cells and lymphocytes); sometimes calculi form
- Sometimes pseudocyst formation
- No true epithelial lining, full of hemorrhagic material filled w/ pancreatic enzymes
- Gross - atrophic, hard, shrunken, dilated ducts and calcified concentrations
10
Q
Dx of Acute Pancreatitis
A
- 1- elevated amylase or lipase (>3X ULN)
- 2- classic ab pain (acute, upper, radiates to back, nausea/vomiting)
- 3- CT showing peri-pancreatic haziness
NEED 2/3
11
Q
How often is acute pancreatitis severe? 3 risks and what defined severe?
A
- 80% mild and 20% severe but hard to detect; Ranson’s or Glasglow criteria
- 3 risks of severe - obesity (pro-inflamm adipokines), alcohol, MCP-1 polymorphism
- Severity is defined by persistent organ failure; SIRS (systemic inflammatory response system) –> vascular leak –> shock, low PaO2, and in creatinine from renal prob)
12
Q
Local and Systemic Complications of Acute Pancreatitis
A
- Local Complications
- Fluid collection w/o wall or fibrous tissue –>pseudocyst (wall but no epithelial layer) in 4 wks
- Pancreatic necrosis w/ fluid and solid debris; seen as un-perfused area w/ CT contrast
- Occurs in 3-5% pts and 20% of these become infected and septic (late cause of death)
- Systemic Complications
- Hypotension, shock, pericardial effusion, EKG changes
- Hypoxia, pleural effusion, ARDS
- Oligouria, azotemia, ATN, renal artery or vein thrombosis
- Hypocalcemia, hyperglycemia (lack of insulin), metabolic acidosis
- Vascular thrombosis and DIC
13
Q
Acute Pancreatitis Tx (mild v severe)
A
- Pancreatic rest (no oral intake) & IV narcotics for pain
- If mild… aggressive IV fluids; esp when first present b/c most at risk for hypovolemia in first 12 hrs
- ID cause - stop alcohol, smoking, drug, remove stones (ERCP), remove gallbladder
- If severe … ICU; may need vent or pressors; NJ tube for nutrition (bypass stomach and duodenum which may be inflammed); prophylactic abx (carbapenems for good pancreas penetration and fluconazole) if >30% necrosis to prevent infected necrosis and septic shock
14
Q
Causes of Chronic Pancreatitis
A
- Same primary etiologies - alcohol abuse, long-term obstruction of ducts AND genetics
- Cystic Fibrosis (CFTR mutation) - pancreatic insufficiency b/c dec bicarb sec
- SPINK1 mutation - inc risk of acute pancreatitis becoming chronic pancreatitis b/c normally inhibits trypsin
- Hereditary Pancreatitis (auto dom) - PRSS1 mutation so cationic trypsin does not self-destruct (inc activation and dc inactivation of trypsin)
15
Q
Chronic Pancreatitis Dx
A
- Structural - CT or EUS showing cysts, dilated ducts, atrophy, stenosis (rarely biopsy)
- Functional tests (most sensitive is “tubed secretin test” - IV secretin then meas duodenal fluid); Large functional reserve so functional tests not pos until late in disease
